An animal study published in the journal Immunity suggests that a ketogenic diet may reduce inflammation in the respiratory tract, helping people with asthma breathe more easily. The researchers put asthmatic mice on a diet that contained mainly fats, but hardly any carbohydrates or proteins—also known as the ketogenic diet.
When a person has an asthma attack, the bronchi become inflamed, accompanied by an increase in mucus production, which makes breathing even more difficult. A central role here is played by cells of the innate immune system, which are called Innate Lymphoid Cells (ILC). They perform a protective function in the lungs by regenerating damaged mucous membranes. For this purpose, they produce inflammatory messengers from the group of cytokines, which stimulate the division of the mucosal cells and promote mucus production.
This mechanism usually is very useful: It allows the body to quickly repair damage caused by pathogens or harmful substances. The mucus then transports the pathogens out of the bronchial tubes and protects the respiratory tract against re-infection. “With asthma, however, the inflammatory reaction is much stronger and longer than normal,” said Christoph Wilhelm of the Institute for Clinical Chemistry and Clinical Pharmacology at the University of Bonn, in a university press release. The consequences are extreme breathing difficulties, which can even be life-threatening.
With the ketogenic diet, the cell metabolism changes: The cells now get the energy they need from burning fat. However, this means that they lack fatty acids, which they need for the formation of new membranes during cell division.
As a result, the division activity of the ILCs in rodents fed a special diet decreased dramatically. “Normally, contact with allergens increases the number of ILCs in the bronchi fourfold,” said Wilhelm. “In our experimental animals, however, it remained almost unchanged. Both mucus production and other asthma symptoms decreased accordingly.”
This is not only due to the switch to fats as an alternative energy source and the resulting shortage of fatty acids; the glucose deficiency presumably also directly contributes to the reduced activity of the ILCs.